Evidence map›Paper›PMID 37658928›Full record

ArticleMolecular biology reports2023

Engineering HEK293T cell line by lentivirus to produce miR34a-loaded exosomes.

Sahar Abdi Sarkami, Sajjad Molavipordanjani, Saeed Abediankenari, Javad Akhtari, Pooria Gill, Hossein Ghalehnoei, Shabanali Khodashenas Lemoni

Abstract read
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In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 36% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Sahar Abdi SarkamiDepartment of Medical Biotechnology, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Sajjad MolavipordanjaniPharmaceutical Sciences Research Center, Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran.
Saeed AbediankenariDepartment of Medical Nanotechnology, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, FarahAbad Road, Sari, Iran.
Javad AkhtariDepartment of Medical Nanotechnology, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, FarahAbad Road, Sari, Iran.
Pooria GillDepartment of Medical Nanotechnology, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, FarahAbad Road, Sari, Iran.
Hossein GhalehnoeiDepartment of Medical Nanotechnology, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, FarahAbad Road, Sari, Iran.
Shabanali Khodashenas LemoniDepartment of Medical Nanotechnology, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, FarahAbad Road, Sari, Iran. S.khodashenas@mazums.ac.ir.
Mazandaran University of Medical Sciences · IR

Funding

Mazandaran University of Medical Sciences 2837
6 · The paper itself

Abstract

backgroundRNA (ribonucleic acid) antisense is developing as a possible treatment option. As an RNA, miR-34a is involved in P53 function and cancer cell apoptosis. Although the therapeutic applications of miRNAs have several limitations, such as structural instability and susceptibility to nucleases. To resolve these issues, this study aims to apply exosomes as a delivery vehicle for miR-34a.

aimsThis study aims to create a cell factory to generate miR34a-enriched exosomes. The produced nanoparticles act as a delivery system and improve the structural stability of miR34a.

methodsFirst exosome specific sequences were inserted into miR34a. The resulting miR34a oligonucleotide was transduced HEK293T cells genome with a lentiviral system. In the structure of miR34a oligonucleotide, six nucleotides were substituted to increase its packaging rate into exosomes. To maintain the secondary structure, stability, and expression of the miRNA gene, changes to the miR34a oligonucleotide were made using PCR (polymerase chain reaction) Extension. The forward-34a (5-TGGGGAGAGGCAGGACAGG-3) and Reverse-34a primers (5-TCCGAAGTCCTGGCGTCTCC-3) were used for amplification of the miR34a gene from DNA.

resultsThe results confirmed that the changes in miR34a oligonucleotide do not affect its secondary structure. The energy level of the manipulated miR34a oligonucleotide was kept the same compared to the original one. Moreover, the loading of miR34a to the exosomes was increased.

conclusionOur findings revealed that normal HEK293T did not express miR34a. However, lentiviral transduced miR34a oligonucleotide induced the loading of miR34a into the exosome. Moreover, replacing six nucleic acids in the 3' end of miR34a increased the loading of miR34a to exosome.

Indexed as

ExosomesMicroRNAsHEK293 CellsHumansLentivirusOligonucleotidesMicroRNAsOligonucleotidesExosomeHEK293TLentiviral vectormiR34a

Identifiers

PMID37658928
OpenAlexW4386387766

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.